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medical microbiology > Gram negative bacteria > Flashcards

Gram negative bacteria Flashcards

1
Q

what makes bacteria gram negative?

A

Cell wall contains lipid A

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2
Q

clinical manifestations associated with the lipid A in cell wall

A

fever, vasodilation, inflammation, shock and DIC (disseminated intravascular coagulation)

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3
Q

DIC (disseminated intravascular coagulation)

A

formation of blood clots within blood vessels throughout the body.

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4
Q

Enterobacteriaceae found in humans and environment

A

Enteric bacteria- members of intestinal microbiota of humans and animalsUbiquitous in water, soil and decaying vegetation

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5
Q

structure of Enterobacteriaceae

A

Coccobacilli or bacilli – 1μm x 1.2-3μmIf motile – peritrichous flagellaSome have prominent capsule, others loose slime

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6
Q

physiology of Enterobacteriaceae

A

All reduce nitrate to nitriteFerment glucose anaerobically – although grow better aerobicallyAll oxidase negative

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7
Q

Enterobacteriaceae Pathogenicity

A

Outer membrane lipopolysaccharide – 3 main antigenic componentsa) core polysaccharide shared by all enteric bacteria-common antigenb) O polysaccharide- various antigenic varieties among strains and species e.g. Salmonella spc) Lipid A

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8
Q

virulence factors x7

A

Lipid A

Capsules

Fimbriae

Exotoxins

Iron binding compounds

Haemolysins

Type III secretion system

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9
Q

Opportunistic coliforms x6

A

E.coli

Klebsiella sp

Serratia sp

Enterobacter sp

Hafnai sp

Citrobacter sp

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10
Q

Opportunistic noncoliform x4

A

Proteus spMorganella spProvidencia spEdwardsiella sp

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11
Q

Truly pathogenic Enterobacteriaceae x3

A

Salmonella spShigella spYersinia spNot considered members of normal microbiota of humans – almost always pathogenic due to their virulence factorsAll 3 synthesize type III secretion systems

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12
Q

salmonella characterics

A

Gram-negative facultatively anaerobic predominantly motile by peritrichous flagellaover 2200 strains identifiedall species are pathogenic to both humans and other animalscomplex cycle of transmission

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13
Q

four main reservoirs of salmonella bacteria

A

intestinal tract of birds and animalssewage, fertilisers and slurryanimal feedshuman carriers

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14
Q

foods typically associated with salmonella contamination

A

meat and meat productsmilk and milk productseggs and egg productsfishconfectionerymiscellaneous foods - dried yeast, frogs legs, marijuana, peanut butter

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15
Q

clinical manifestation of Enteritis (salmonella infection caused) x6

A

diarrhoea, abdominal pain, mild fever, chills, nausea, vomiting

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16
Q

incubation period and infection dose of salmonella

A

incubation period of 5-72 hours, but occasionally up to 7 dayslasts 2-5 daysinfective dose varies from as little as 50 cells to 1,000,000 per gram of food

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17
Q

Enteric Fevers

A

some species can cause more serious infections eg. S. typhi and S. paratyphi.

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18
Q

pathogenicity of salmonella

A

Salmonellae adhere to the epithelial lining of the ileum by means of fimbriae followed by invasion and multiplication

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19
Q

toxins produced salmonella

A

endotoxin3 enterotoxinscytotoxin

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20
Q

prevention of salmonella outbreaks

A

joint action by agriculture and food sectors by the consumer control starts on the farm and continues through the food chain to the consumer

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21
Q

S.typhi infection

A

Humans sole hostsInfection via ingestion of contaminated food or water

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22
Q

spread of S.typhi infection through body

A

Bacteria pass through intestinal wall to bloodstreamPhagoscytised but not killed and carried to liver, spleen, bone marrow & gallbladder

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23
Q

clinical manifestations of S.typhi infections

A

Patients have increasing symptoms of fever, headache, malaise, muscle pain & loss of appetite – lasts about a weekBacteria released from gallbladder to re-infect the intestines – resulting in gastroenteritis abdominal pain & recurring bacteremiaIn some bacteria ulcerate and perforate intestinal wall causing peritonitis in abdominal cavity.

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24
Q

Escherichia coli taxonomy

A

Domain- Bacteria Phylum- Proteobacteria Class- Gammaproteobacteria Order- Enterobacteriales Family- Enterobacteriaceae

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25
Q

diseases associated by E coli x4

A

UTI’sNeonatal meningitisGastroenteritisSevere to fatal hemorrhagic colitis

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26
Q

Gastroenteritis caused by e coli

A

exotoxin called enterotoxin bind proteins on intestinal tract cell lining portion enters cell and triggers a series of chemical reactions results in loss of electrolytes producing watery d & v – a common cause of paediatric infections on developing countries.

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27
Q

hemorrhagic colitis

A

enterohemorrhagic E coli, or EHEC - most notably O157:H7produce relatively large amounts of the bacteriophage-mediated Shiga-like toxin. This toxin is called Vero toxin (VT), or Vero cytotoxin after its cytotoxic effect on cultured Vero cells. Many strains of O157:H7 also produce a second cytotoxin (Shiga-like toxin 2, or Vero toxin 2), which is similar in effect but antigenically different.

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28
Q

treatment of e coli infections

A

supportive treatment - dehydration various antimicrobials ( carefully selected as some will worsen the symptoms as lysed bacteria release exotoxin )

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29
Q

prevention of e coli infection

A

prevent faecal contamination of food and water good personal hygiene

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30
Q

shigella

A

Genus of Gram-negative, non-spore forming rod-shaped bacteria closely related to Escherichia coli and Salmonella.

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31
Q

shigellosis

A

caused by shigella infection only in primates

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32
Q

Serogroup A: S. dysenteriae (12 serotypes)

A

S. dysenteriae is usually the cause of epidemics of dysentery, particularly in confined populations such as refugee camps.

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33
Q

Serogroup B: S. flexneri (6 serotypes)

A

S. flexneri is the most frequently isolated species worldwide accounts for 60% of cases in the developing world;

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34
Q

Serogroup C

A

S. boydii(23 serotypes)

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35
Q

Serogroup D: S. sonnei (1 serotype)

A

S. sonnei causes 77% of cases in the developed world

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36
Q

Pathogenesis of shigella infection

A

Shigella infection is typically via ingestion (fecal–oral contamination); depending on age and condition of the host as few as ten bacterial cells can be enough to cause an infection. causes dysentery that results in the destruction of the epithelial cells of the intestinal mucosa in the cecum and rectum.

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37
Q

toxins produced by shigella

A

Some strains produce enterotoxin & Shiga toxin, similar to the verotoxin of E. coli O157:H7. Both Shiga toxin and verotoxin are associated with causing hemolytic uremic syndrome.

38
Q

The Shigella chromosomes

A

share most of their genes with that of E. coli K12 strain MG1655

39
Q

Shigella genomes includes a virulence plasmid

A

Each of the Shigella genomes includes a virulence plasmid that encodes conserved primary virulence determinants.

40
Q

treatment of shigella infection

A

Replacing fluids & electrolytes
Oral antibiotics can be given to reduce the spread in close contacts e.g.Ciprofloxacin & cephalosprins
Vaccine (live attenuated) being developed with some success against S.flexneri

41
Q

Yersinia species x3

A

Genus contains 3 notable species
Y. enterocolitica
Y. pseudotuberculosis
Y. pestis

42
Q

Y. enterocolitica

A

enteric pathogens acquired via consumption of contaminated food or water by animal faeces.
occurs most often in young children.

43
Q

Common symptoms in children

A

fever, abdominal pain, and diarrhea, which is often bloody.
Symptoms typically develop 4 to 7 days after exposure and may last 1 to 3 weeks or longer.

44
Q

In older children and adults,

A

right-sided abdominal pain and fever may be the predominant symptoms, and may be confused with appendicitis due to inflammation of mesenteric lymph nodes

45
Q

Yersinia pestis

A

infectious agent of plague

46
Q

Plague transmission

A

People usually get plague from being bitten by a rodent flea that is carrying the plague bacterium or by handling an infected animal.

47
Q

treatment of plague

A

modern antibiotics are effective against plague, but if an infected person is not treated promptly, the disease is likely to cause illness or death.

48
Q

Bubonic plague

A

painful swollen lymph nodes
bacteremia results in DIC, subcutaneous hemorrhaging & tissue death
‘Black Death’

49
Q

Pneumonic plague

A

pulmonary distress within a day
can spread person to person via aerosols & sputum

50
Q

Oxygen is essential for

A - obligate aerobes

B - obligate anaerobes

A

A

51
Q

Why is oxygen is essential for obligate aerobes?

A

Serves as the final electron acceptor in electron transport chains which produce most of the ATP in these organisms.

By contrast oxygen is a deadly poison for obligate anaerobes

52
Q

How can oxygen be essential for one group of organisms and yet be a fatal toxin for others?

A

Neither gaseous atmospheric oxygen (O2) nor the covalently bound oxygen in compounds such as carbohydrates or water is poisonous
The forms of oxygen that are toxic are those that are highly reactive.

53
Q

Why are highly reactive forms of oxygen toxic?

A

because in the same way that oxygen is the final oxygen acceptor for aerobes, they are excellent oxidizing agents,
i.e. they steal electrons from other compounds

54
Q

How toxic forms of oxygen cause a chain reaction that damages cells?

A

The electron depleted compounds then steal electrons from other compounds
Resulting in a chain of vigorous oxidation
Causing irreparable damage to cells by oxidising important compounds including proteins and lipids

55
Q

Singlet oxygen (1O2)

A

toxic form of oxygen - A very reactive oxidizing agent

Molecular oxygen – electrons boosted to a higher energy state – during aerobic metabolism

Phagocytic cells – certain human white blood cells use it to oxidize pathogens

56
Q

Superoxide radical (O2-)

A

Superoxide radicals form

  • during incomplete reduction of O2 during electron transport in aerobes
  • during metabolism by anaerobes in the presence of oxygen
57
Q

How aerobic organisms detoxify superoxide radicals

A

Produce superoxide dismutase – lacking in anaerobes

Have active sites that contain metal ions e.g. Zn2+ and Fe2+

Combine 2 superoxide radicals and 2 protons to form hydrogen peroxide (H2O2) and oxygen

58
Q

Peroxide anion O22-

A

Hydrogen peroxide produced during reactions catalysed by superoxide dismutase

Peroxide anion makes hydrogen peroxide an antimicrobial agent

59
Q

What do aerobes have to detoxify the peroxidase anion?

A

either catalase or peroxidase

60
Q

Hydroxyl radical (OH)

A

Hydroxyl radicals result from ionising radiation and from incomplete reduction of hydrogen peroxide

61
Q

What is the most reactive of the 4?

A

Hydroxyl radicals

Due to catalase and peroxidase effect eliminated in aerobes

62
Q

other antioxidants aerobes can use

A

Vitamin C & E

Again, provide electrons that reduce toxic forms of oxygen

63
Q

Facultative anaerobes

A

Can live in various oxygen concentrations

64
Q

How do facultative anaerobes maintain life

A

Can maintain life via fermentation or anaerobic respiration

65
Q

Metabolic efficiency in absence of oxygen for facultative anaerobes

A

reduced

66
Q

Example of facultative anaerobe

A

E.coli

67
Q

Aerotolerant anaerobes

A

Do not use aerobic metabolism

Have some detoxifying enzymes

68
Q

example of a Aerotolerant anaerobe

A

lactobacilli

69
Q

Microaerophiles

A

Microaerophiles are damaged by the 21% concentration of atmospheric oxygen

Some organisms require oxygen levels of 2% to 10%

70
Q

Example of microaerophile

A

Helicobacter pylori

ulcer causing pathogen

concentration of oxygen in stomach 2-10%

71
Q

Injecting Drug User (IDU) Infections

A

40% of IDU hospital admissions due to infections, 20% result in death

Intravenous, intra-muscular or subcutaneous injection

Minor bacterial infections usually result in local abscess formation

72
Q

Severe IDU infections

A

Severe illness if the injected material or paraphernalia, are contaminated with certain clostridial spores

73
Q

Clostridia

A

Gram positive anaerobic spore-forming rods

74
Q

Where is Clostridia found?

A

Widely distributed in soil and gut

75
Q

How does Clostridia exist?

A

exo-spores

Resistant to environmental conditions

Spores germinate when introduced into an oxygen-reduced environment

76
Q

Pathogenic Clostridia species

A
  • C. perfringens*
  • C. septicum*
  • C. sordellii*
  • C. novyi*
  • C. histolyticum*
  • C. tetani*
  • C. botulinum*
  • C. difficile*
77
Q

IDU Outbreak, 2000

A

Cases of serious illness and deaths amongst IDUs recorded in parts of UK

60 IDUs in Scotland acquired a severe infection at or near an injection site

78
Q

clinical manifestations of IDU outbreak

A

Spread rapidly

Extensive skin and muscle damage

Hypotension

Multi-organ failure

23 deaths

79
Q

origin of IDU outbreak

A

Association with a batch of heroin in circulation at the time and the practice of skin or muscle “popping”

80
Q

Clinical Presentation of Clostridia infection; Soft tissue inflammation at injection site

A

Abscess, Cellulitis, Fasciitis, Myositis

81
Q

Clinical Presentation of Clostridia infection; Local inflammatory reaction has varied

A

Minimal pain and swelling at injection site

82
Q

Clinical Presentation of Clostridia infection; Severe local symptoms

A

Extensive swelling, Pain, Oedema, Erythema with blackening/blistering at centre, Extensive necrosis, Necrotising fasciitis

83
Q

C.novyi Type A

A

Widely distributed in soil

Gram-variable rods, some with sub-terminal spores

84
Q

Identifying C.novyi Type A

A

Examine anaerobic cultures after 24h incubation for small, flat, rough or rhizoidal, translucent, haemolytic colonies with a spreading edge

Exposure to air toxic to micro-colonies that haven’t begun sporulation

After 48-72h, colonies often coalesce to give a fine spreading growth

Unreactive in commercial anaerobe identification kits (API Anaerobe)

85
Q

C.perfringens

A

Post-mortem contaminant

Straight-sided, gram variable rods, no spores

86
Q

Identifying C.perfringens morphological appearance

A

Large discrete colonies after 24h incubation

Flat and rough-edged, or smooth and domed

Non-haemolytic or with a narrow zone of complete haemolysis inside a larger zone of partial haemolysis

87
Q

C.septicum

A

Gram variable rods, numerous sub-terminal spores

Most common source of isolates from blood cultures of patients with malignancies of the colon

88
Q

Culture growth of C.septicum

A

Grows rapidly

Thick, swarming growth, haemolytic

89
Q

C.botulinum

A

Profuse sub-terminal and free spores, gram variable bacilli

Implicated in food-borne illnesses and cases of wound botulism

90
Q

Culture growth of C.botulinum

A

Proteolytic types A,B and F initially produce discrete rhizoidal colonies that spread and coalesce

Haemolysis is variable

91
Q

C.tetani history in human disease

A

Uncommon in recent decades

Outbreak between July ‘03 and March ‘04, 22 cases in IDUs

92
Q

Culture growth and identification of C.tetani

A

Colonies may produce a fine swarming growth

Gram stain of overnight cultures can give readily over-decolorised long bacilli without spores

Classical ‘drumstick’ appearance of cells with terminal, round spores after further incubation

medical microbiology (29 decks)

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